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Journal of Neuroscience Nursing:
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Acute Ischemic Stroke Review

Hinkle, Janice L.; Guanci, Mary McKenna

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Author Information

Questions or comments about this article may be directed to Janice L. Hinkle, PhD RN CNRN, at janice.hinkle@ndm.ox.ac.uk. She is a senior research fellow funded by the Medical Research Council at the University of Oxford Acute Stroke Programme in the Nuffield Department of Clinical Medicine, John Radcliffe Hospital, Headington, Oxford, England.

Mary McKenna Guanci, MS RN CNRN, is a clinical nurse specialist in the Neuroscience Intensive Care Unit at Massachusetts General Hospital, Boston, MA.

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Abstract

More than 700,000 people have a stroke each year in the United States. A diagnosis of stroke formerly elicited a nihilistic approach, but this has substantially changed in the last decade. Currently, time is brain, and it is important for all disciplines to work together to initiate acute stroke protocols in the emergency department and identify patients within the therapeutic time window for thrombolytic and neuroprotective therapies. Evolving protocols, management, and nursing care all have important implications during the acute phase of ischemic stroke. Patient and family education on risk reduction must also be addressed by the entire healthcare team.

Stroke is the third leading cause of mortality in the United States. Of the approximately 700,000 strokes occurring each year, about 550,000 are first strokes. About 400,000 strokes are ischemic (Thom et al., 2006). Stroke is the leading cause of adult disability with more than 4 million stroke survivors in the United States alone. Approximately 90% of stroke survivors are left with some residual deficit.

In 1994 the Stroke Council of the American Heart Association (AHA) published the first guidelines for the management of acute ischemic stroke (Adams et al., 1994). In 1996, the U.S. Food and Drug Administration (FDA) approved intravenous (IV) tissue plasminogen activator (tPA) as the first medication to treat acute ischemic stroke. The AHA subsequently published a supplement to the 1994 guidelines that addressed tPA (Adams et al., 1996). The advent of new therapies for acute ischemic stroke has brought about higher expectations for improved recovery and good outcome (Demchuk & Buchan, 2000). The AHA published guidelines for the early management of ischemic stroke in 2003 (Adams et al., 2003) and updated them in 2005 (Adams, Adams, del Zoppo, & Goldstein, 2005) and in 2007 (Adams et al., 2007).

This article reviews the pathophysiology of acute ischemic stroke and related patient care, identifies the laboratory and diagnostic tests the neuroscience nurse can expect to see in the fast‐paced evaluation of a patient following an ischemic stroke, addresses the medical and nursing management approaches with which the neuroscience nurse needs to be familiar during the acute phase of the inpatient stay for ischemic stroke, and reviews patient and family education topics that must be addressed by the healthcare team.

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Pathophysiology

Stroke is defined as an “acute neurologic dysfunction of vascular origin with sudden (within seconds) or at least rapid (within hours) occurrence of symptoms and signs corresponding to the involvement of focal areas in the brain” (Goldstein, Barnett, et al.,1989, p. 1412). The two main types of stroke are ischemic and hemorrhagic, accounting for approximately 85% and 15%, respectively (Hickey, 2003).

When an ischemic stroke occurs, the blood supply to the brain is interrupted, and brain cells are deprived of the glucose and oxygen they need to function. Ischemic stroke is a complex entity with multiple etiologies and variable clinical manifestations. Approximately 45% of ischemic strokes are caused by small or large artery thrombus, 20% are embolic in origin, and others have an unknown cause (Hickey, 2003).

Thrombosis can form in the extracranial and intracranial arteries when the intima is roughened and plaque forms along the injured vessel. The endothelial injury (roughing) permits platelets to adhere and aggregate, then coagulation is activated and thrombus develops at site of plaque. Blood flow through the extracranial and intracranial systems decreases, and the collateral circulation maintains function. When the compensatory mechanism of collateral circulation fails, perfusion is compromised, leading to decreased perfusion and cell death.

During an embolic stroke, a clot travels from a distant source and lodges in cerebral vessels. Microemboli can break away from a sclerosed plaque in the carotid artery or from cardiac sources such as atrial fibrillation, patent foramen ovale, or a hypokinetic left ventricle (Hickey, 2003). Emboli in the form of blood, fat, or air can occur during surgical procedures, most commonly during cardiac surgery, but also after long bone surgeries (Warlow et al., 2001).

Less common causes of ischemic stroke include carotid dissection (Bader & Littlejohns, 2004) and the presence of coagulopathies, such as those resulting from antiphospholipid antibodies (APASS Investigators, 2004). Other causes include arteritis, infection, and drug abuse, such as the use of cocaine (Blank‐Reid, 1996; Hickey, 2003). While still not completely understood, the presence of periodontal disease and tooth loss is also an associated risk for ischemic stroke (Joshipura, Hung, Rimm, Willett, & Ascherio, 2003).

As a thrombosis or emboli cause a decrease in blood supply to the brain tissue, events occur at the cellular level, referred to as the ischemic cascade. Neurons and support cells require a careful balance of variables such as temperature, pH, nutrition, and waste removal in their environment to function optimally (Hinkle & Bowman, 2003). Intensive basic scientific research during the last two decades has given healthcare professionals an increased understanding of the ischemic cascade in the format of the precise environmental alterations involved in the pathophysiology of ischemic injury at the cellular level. Understanding the ischemic cascade has led to the concept of a therapeutic time window for treatment possibilities. Often, there is a core region of dead cells surrounded by an area of hypoperfused tissue. The hypoperfused area may be rescued; this area is referred to as the penumbra region (Muir, Buchan, von Kummer, Rother, & Baron, 2006). Neuroprotection is a broad term that refers to pharmacological and nonpharmacological treatments used to halt the cellular events in the ischemic cascade, forming the theoretical basis for many of the acute stroke therapies under study (Lees et al., 2006) as well as the rationale for intervening within a therapeutic time window following ischemic stroke.

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Initial Assessment

Assessment of the patient with a stroke begins with recognition of the event as a stroke in the prehospital phase of care and continues throughout care. Emergency medical technicians and ambulance staff members need training in the recognition of signs and symptoms of stroke. Tools such as the Face Arm Speech Test (Harbison et al., 2003) and the shortened National Institutes of Health Stroke Scale (sNIHSS; Tirschwell et al., 2002) have been tested and found to be effective in increasing the diagnostic accuracy of ambulance staff. The National Association of EMS Physicians has published standards for acute stroke prehospital care (Sahni, 2000) which the AHA did not seek to duplicate but continued to emphasize the need for immediate diagnosis and evaluation (Adams et al., 2003).

In the emergency department (ED), as the patient arrives, preferably by ambulance, a suspected stroke is treated as an acute event until diagnostic evidence suggests otherwise. Neurological assessment is based on both subjective and objective data, and a careful medical history is crucial to establish the exact time of onset of stroke signs and symptoms. Essential data to include are a quick history of timing of the event, pertinent past medical history, and risk factors. The full NIHSS (Fig 1) can be used to guide the neurologic assessment (Goldstein, Bertels, & Davis, 1989; Goldstein & Samsa, 1997; Richardson, Murray, House, & Lewenkopf, 2006).

Fig 1
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Symptoms of ischemic stroke according to the areas of cerebral circulation are shown in Figure 2. In addition to these symptoms, determining dominance is important as the dominant hemisphere is primarily responsible for language function. Handedness determines dominance for most people. Right‐handed people are left‐hemisphere dominant; left‐handed people are also left‐hemisphere dominant about 60% of time. The clinical features that are more common with a dominant left cerebral hemisphere lesion include aphasia, agraphia, acalculia, apraxias, a left gaze preference, a right visual field deficit along with right‐sided hemiparesis, and a right‐sided hemisensory loss. Common features of a nondominant right cerebral hemisphere include neglect (left‐sided hemiinattention), right gaze preference, left visual field deficit, dysarthria, flat affect, left‐sided hemiparesis, and left‐sided hemisensory loss (Bader & Littlejohns, 2004; Hickey, 2003).

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The presence of a transient ischemic attack or other conditions need to be ruled out to ensure that patients receive the appropriate treatment for their condition (Tietgen, 2005; Townend, Hanson, Sturm, & Whyte, 2005). A wide range of abnormalities can mimic a stroke, including hypoglycemia, migraine, seizure, and trauma (Fig 3).

Fig 3
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Diagnostic studies help to confirm stroke, detect early potentially life‐threatening complications, and direct specific care given; those recommended in the AHA guidelines are shown in Figure 4 (Adams et al., 1994; Adams et al., 2003; Adams et al., 2007). These diagnostic tests are available in most EDs 24 hours a day. Blood glucose can be checked in the ambulance with a finger stick or upon ED arrival and is helpful in ruling out hypoglycemia as a cause for the event or hyperglycemia as a compounding factor. A computed tomography (CT) scan without contrast is recommended to rule out the presence of a hemorrhagic stroke that would preclude the use of thrombolysis (Muir et al., 2006). Adjunct studies may include a CT angiogram, magnetic resonance imaging (MRI), and cerebral angiography. A CT angiogram can be used to identify large vessel stenoses or occlusion. MRI allows for better visualization of possible infarcted areas, and angiography is used when intraarterial (IA) thrombolysis is indicated or when surgical interventions are being considered.

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Acute Stroke Teams

An element critical to the success of stroke treatment is the formation of an acute stroke team that will guide all patients through the hyperacute and acute phases of stroke care (Bonnono et al., 2000; Rapp et al., 1997). Team members include emergency medical services (EMS) personnel, ED staff members, intensive care unit (ICU) staff members, stroke physicians, radiologists or neuroradiologists, interventionalists, staff nurses from additional areas as needed, and others. Most stroke teams follow treatment protocols, guidelines, standing orders, or pathways and prospectively collect data for review to provide guidance and refine future stroke care (Holloway, Vickrey, Benesch, Hinchey, & Bieber, 2001).

The nursing focus is on patient assessment, blood pressure management, injury prevention, prevention of complications such as aspiration, and other aspects of care. Early blood pressure management is critical to prevent further ischemic injury during acute stroke. The American Stroke Association (ASA) has recommendations for blood pressure (BP) management, which are shown in Table 1. The recommendations differ according to whether the patient is eligible for thrombolysis and according to their BP measurement.

Table 1
Table 1
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The advent of thrombolytic therapy has been responsible for driving the current acute stroke protocols. Eligibility criteria for IV thrombolysis therapy must be met before administration of a thrombolytic drug. Criteria for tPA are shown in Figure 5 (Bader & Littlejohns, 2004; Kongable, 1997). IV tPA must be initiated within 3 hours of symptom onset. If the BP or blood glucose values are not within the criteria but can be brought within the recommended ranges within the 3‐hour window, tPA can be administered. The tPA dose is 0.9 mg/kg, not to exceed 90 mg. It is administered by a 10% bolus followed by the remaining 90% of the dose infused during the next hour.

Fig 5
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Nursing care for a patient during and after IV tPA infusion includes neurologic assessment every 15 minutes for 2 hours and then every 30 minutes for 6 hours to include monitoring for signs and symptoms of intracerebral hemorrhage (ICH). If a decrease in the level of consciousness or worsening neurologic deficit occurs during infusion, notify the physician and stop the infusion. There is a 50% mortality rate associated with ICH. The patient should be monitored for gastrointestinal or genitourinary hemorrhage or bleeding at puncture sites. Bleeding precautions should be instituted that include monitoring the patient in an ICU or stroke unit and avoiding placement of a nasogastric tube, indwelling bladder catheter, or IA pressure catheters in the first 24 hours following tPA administration (Adams et al., 2003).

The ability to deliver IA tPA extends the possible acute‐therapy window from 3 hours to 6‐12 hours for selected patients (Adams et al., 2003). The IA route for tPA is a treatment consideration when rapid recanalization is desired. IA tPA must be given within 6 hours of onset of anterior stroke symptomatology and within 12 hours of onset of posterior circulation stroke symptoms. The immediate nursing concerns are similar to those of IV tPA with the additional concern of the possibility of a retroperitoneal bleed or groin hematoma when a femoral access is used for catheterization and medication delivery (Adams et al., 2003). The need to provide adjunct therapies to maintain vessel patency after an arterial procedure may complicate this therapy. These therapies may include heparin administration to prevent acute reocclusion and use of IIb/IIIa receptor antagonists (Intregrilin) to prevent acute reocclusion and endothelial injury, especially if a stent has been used. Bridging therapy is a term used to describe the use of both IV tPA and IA tPA. This approach is used when telemedicine is used to treat stroke in areas without neurointerventional teams available (LaMonte et al., 2003). A patient may receive IV tPA at the transferring hospital followed by IA tPA when they reach a hospital with a neurointerventional team qualified to administer IA therapy.

Anticoagulation is often used to prevent recurrent stroke. Traditional anticoagulants, such as IV heparin followed by oral warfarin sodium (Coumadin), may be used to prevent an early recurrent embolus, assist in maintaining collateral blood flow, and halt progression of additional thrombus by interfering with the clotting cascade. Antiplatelet agents such as aspirin, ticlopidine hydrochloride (Ticlid), dipyridamole (Persantine), and IIb/IIIa receptor antagonists are used to inhibit platelet aggregation for secondary stroke prevention.

The goals of acute stroke care are to support recovery, prevent complications, prevent recurrent stroke, and ensure that the patient reaches the highest possible functional outcome. This requires an interdisciplinary approach with nurses playing a major role in all aspects of care. Admission of the patient to a stroke unit is a highly rated and an agreedupon performance measure that helps all disciplines meet these goals (Adams et al., 2003; Holloway et al., 2001).

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Preventing Acute Complications

Supportive care includes continuous assessment of airway, ventilatory support, and supplemental oxygen to maintain a pulse oximetry level >92% (Adams et al., 2007). Normothermia is promoted as fever has been associated with poor outcome after stroke. The patient is monitored for cardiac arrhythmia (Adams et al., 2007).

Although the optimal management of acute arterial hypertension has not been established, there is little scientific basis and no clinically proven benefit for lowering BP (Adams et al., 2007). The consensus is that antihypertensive agents should be withheld unless the diastolic BP is >120 mm Hg or the systolic BP is >220 mm Hg (Table 1).

Medical interventions are used to induce hypertension in some centers to maintain perfusion to an ischemic area. A combination of volume expansion with albumen and intravenous medications such as phenylephrine (Neo‐Synephrine) may be used to increase blood pressure and augment cerebral blood flow in an attempt to improve the patient's neurologic status (Adams et al., 2005; Rordorf, Koroshetz, Ezzeddine, Segal, & Buonanno, 2001). The patient also needs to be monitored in an ICU for hypotension, and the BP must be supported with appropriate medications if needed.

Surgical interventions for stroke depend on the exact pathology. Hemicraniectomy may be used to control increased intracranial pressure that occurs from cerebral edema following a large hemispheric stroke. Other surgical interventions, such as carotid endarterectomy or extracranial/intracranial bypass, can help increase brain perfusion; however, such procedures are rarely performed during the acute phase of care as they are measures to prevent secondary stroke. Neurointerventional procedures in the treatment of stroke include angioplasty and carotid stenting. Angioplasty, with or without carotid stenting, may be used to improve perfusion to areas of the brain at risk. The FDA has approved a clot retrieval device that has been used in a small number of cases to restore perfusion (Felton et al., 2005). Research on clinical outcomes continues.

Neurologic examination of the patient is of vital importance particularly in the acute phase of care. The exam includes observation for changes in the patient before, during, and after therapies. Frequent nursing assessment is necessary because of the risk of increasing intracranial pressure from ICH, reperfusion injury, and cerebral edema. The NIHSS is a useful tool for assessment as it is a standardized neurologic examination intended to describe the neurologic deficits in patients with stroke, and it is reliable and valid when used by physicians and nurses (Goldstein, Bertels, et al., 1989; Goldstein & Samsa, 1997). It does not, however, contain all the components of a neurologic exam, so it cannot be used exclusively. Additional neurologic assessment needs to include assessment of size and reactivity of pupils and cranial nerves (American Association of Neuroscience Nurses [AANN], 2004).

BP management within the prescribed goals is critical to prevent secondary complications (Table 1). BP goals are dependent upon stroke etiology and individual risks. Observations for changes in the neurologic exam with BP manipulation are vital in achieving therapeutic goals.

Glycemic control is needed to prevent increase in infarction size and edema and to lower recanalization rates that can occur with acute and chronic hyperglycemia (Ribo et al., 2005). Hypoglycemia can cause further neurologic signs and lead to further brain injury. Blood glucose target range is 80‐120 mg/dL (Adams et al., 2003).

Decreases in level of consciousness, tongue or throat weakness, or a decreased gag reflex may compromise the patient's airway. Nursing interventions that promote an adequate airway include assessment of the patient's ability to clear secretions. Oxygen saturation monitoring is used to evaluate oxygenation levels. The patient is positioned with his or her head midline and the head of bed elevated 30° to decrease risk of aspiration and enhance venous return (AANN, 2004). Chest physical therapy, suctioning, and incentive spirometry help to clear secretions and maintain a patent airway. Ventilator care, including weaning and evaluating for tracheostomy, is important in moving the patient through the continuum of care. An oral care guideline will aid in prevention of ventilator‐associated pneumonia.

Aspiration is a major concern when caring for a patient with stroke because of limited ability to protect the airway and risk of dysphagia. Dysphagia may be caused by decreased level of consciousness or cranial nerve impairment. A swallow screen should be completed before a patient receives anything by mouth, especially water or medications. A swallow screen should include evaluation of level of consciousness, ability to cough, phonation, pharyngeal sensation, and the ability to swallow water. A positive gag reflex should not be interpreted as a valid swallow screen, because patients with intact gag reflexes may not be effectively able to swallow. Insertion of a nasogastric or orogastric tube may be necessary to provide nutrition and medications if a patient fails a preliminary swallow screen. A gastric tube is needed if long‐term impairment is anticipated. Guidelines suggest that a feeding tube should not be inserted for 24 hours after tPA administration because of increased risk of bleeding; however, a patient may need protection if vomiting and aspiration is a concern. Patients should be fed within 48 hours of admission if possible. Keeping the head of the bed elevated at least 30° may aid in preventing aspiration, but this is always done with caution and monitoring to avoid hypotension. A consult with a speech pathologist and a dietitian aids in acute care and rehabilitation planning.

The patient's ability to communicate must also be assessed, particularly after a dominant hemisphere stroke. Communication boards, an enhanced call system, or computers may help the patient communicate needs. Reassurance, reorientation, and education about the present condition and rehabilitation needs are necessary to prepare the patient for discharge. Speech therapists will also assist in the evaluation of communication skills and cognitive status.

Stroke patients often have an alteration in physical mobility related to weakness, immobility caused by disruption of movement pathways, and neglect. This increases the risk of deep vein thrombosis, pulmonary complications such as pneumonia, and falls. Elastic stockings, compression boots, and drugs such as low‐molecular‐weight heparin may be used to prevent deep vein thrombosis. If a patient is on bed rest, monitoring of skin integrity and a turning schedule will help prevent skin breakdown. An evaluation of motor strength, balance, range of motion, and neglect is needed. Early mobilization is recommended, if possible, within the first 48 hours (Holloway et al., 2001). Physical and occupational therapy consults are necessary to evaluate for splinting, further evaluation, and rehabilitation planning. Stroke is a life‐changing event. Optimizing independence is important in the plan of care.

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Secondary Prevention and Education

The patient's stroke risk factors must be assessed, and the patient and family learning needs should be addressed. A baseline assessment of the degree of knowledge deficit related to modifiable risk factors and the need for secondary prevention needs to be conducted. The degree of readiness to change must also be assessed (Miller & Spilker, 2003).

An overview of the recommendations for the secondary prevention of stroke according to the most common risk factors can be found in Figure 6. Hypertension needs to be addressed with the goal of eventually getting the systolic BP lower than 120 mm Hg and diastolic BP lower than 80 mm Hg (National Institutes of Health, 2003; Sacco et al., 2006). Patients with diabetes mellitus must have glucose levels controlled. Cholesterol levels must be evaluated, diet changes made, lipid‐lowering drugs started, and cigarette smoking eliminated. Smokingcessation interventions are most effective when started while the patient is in the hospital (Rice, 2006). Excessive alcohol use should be eliminated. Physical inactivity must be addressed, and the benefits of an exercise program and a healthy diet leading to weight loss in obese individuals should be explained (Sacco et al.).

Fig 6
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When new medications are prescribed for secondary prevention, the patient needs to receive education regarding their indication, duration, monitoring, and potential side effects. Warfarin (Coumadin) is the most common oral anticoagulant used in the treatment of cardiothrombolic stroke in patients with atrial fibrillation. The International Normalized Ratio is used to monitor and maintain anticoagulation in the therapeutic range of 2‐3 (Sacco et al., 2006). Unless contraindicated, aspirin therapy is often recommended if anticoagulation is not used as a treatment strategy, and patients must understand the associated risks for this therapy if prescribed. Further recommendations for the prevention of recurrent stroke in a variety of other circumstances can be found elsewhere (Sacco et al.).

Educational interventions need to be tailored to the individual's education level and learning style (Hickey, 2003; Moore, 2001). Materials tailored to the needs of the patient and family include a wide variety of media. Printed materials on specific medications are available from most hospital pharmacies, many in alternate languages as needed. Videotapes or DVDs on medications and procedures are available for visual learners. Patients who are computer savvy may prefer recommended Web sites, such as the ASA Web site (www.strokeassociation.org) and the National Stroke Association Web site (www.stroke.org). Each patient and family should receive printed materials outlining the warning signs of stroke. These warning signs are available from the ASA in both English and Spanish (ASA, 2000). Printed patient teaching materials about stroke risk factors and modifiable risk factors are also available through the ASA's Get With The Guidelines program, available at www.americanheart.org.

Education concerning rehabilitation needs and support services available may assist the patient and family during recovery. Social work and chaplaincy consults are needed in the support of patients and families. Physiatry and neuropsychiatry can further support the patient's recovery.

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Summary

All healthcare professionals want the best outcomes for people who have had an ischemic stroke. A nihilistic approach toward a patient with a diagnosis of acute ischemic stroke is no longer appropriate. Today's healthcare professionals are aware that it is important for all disciplines to work together to achieve better outcomes for patients by being knowledgeable about early and aggressive evaluation and treatment recommendations. Healthcare professionals also work hard to assure that patients and family members are knowledgeable about stroke prevention. Many important areas of patient teaching begin in the acute setting and continue in the outpatient setting, home or rehabilitation.

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Continuing Education Credit

The Journal of Neuroscience Nursing is pleased to offer the opportunity to earn neuroscience nursing CE for this article online. Go to www.aann.org, and select “Continuing Education.” There you can read the article again or go directly to the posttest assessment. The cost is $15 for each article. You will be asked for a credit card or online payment service number.

The posttest consists of 10 questions based on the article, plus several assessment questions (e.g., How long did it take you to read the article and complete the posttest?). A passing score of 80% (8 of 10 questions correct) on the posttest and completion of the assessment questions yields 1 hour of continuing education in neuroscience nursing for each article.

The American Association of Neuroscience Nurses is accredited as a provider of continuing nursing education by the American Nurses Credentialing Center's Commission on Accreditation.

© 2007 American Association of Neuroscience Nurses

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